The role of the dynamic epigenetic landscape in senescence: orchestrating SASP expression.

Senescence and epigenetic alterations stand out as two well-characterized hallmarks of aging. When cells become senescent, they cease proliferation and release inflammatory molecules collectively termed the Senescence-Associated Secretory Phenotype (SASP). Senescence and SASP are implicated in numerous age-related diseases.

Linked regulation of genome integrity and senescence-associated inflammation by p53.

Genomic instability and inflammation are distinct hallmarks of aging, but the connection between them is poorly understood. Understanding their interrelationship will help unravel new mechanisms and therapeutic targets of aging and age-associated diseases. Here we report a novel mechanism directly linking genomic instability and inflammation in senescent cells through a mitochondria-regulated molecular circuit driven by p53 and cytoplasmic chromatin fragments (CCF).

Photochemotherapy of Infrared Active BODIPY-Appended Iron(III) Catecholates for in Vivo Tumor Growth Inhibition.

Iron(III) catecholates of BODIPY (boron-dipyrromethene)-conjugated dipicolylamine ligands, viz. [Fe(L)(cat)Cl] () and [Fe(L)(cat)Cl] () (Hcat = catechol), with a ligand-to-metal charge transfer band at ∼800 nm were studied for their in vivo activity in dark and infrared light in luciferase-expressing human breast adenocarcinoma (BT474luc) cells. Complex displayed in vitro photocytotoxicity in BT474luc cells (IC: 6 μM) in infrared light of 600-720 nm with moderate dark toxicity (IC: 18 μM) as evidenced from the MTT and Annexin-V FITC/PI staining assays.